Effects of Sepsis on Diaphragmatic Function in Rats

Abstract

The effects of a 3-day pneumococcal infection on diaphragmatic strength and endurance capacity were studied in an in vivo rat model. Thirty-four rats were divided into a control (C)(n = 17) or a septic (S) group (n = 17). Animals were inoculated subcutaneously with 1011 Streptococcus pneumoniae (S), or sterile culture media (C). All rats were studied 3 days after inoculation. Diaphragmatic strength and endurance capacity were studied in 11 animals of each group. Diaphragmatic strength was assessed by measuring transdiaphragmatic pressure (Pdi) generated during electrical stimulation of the phrenic nerves at different frequencies (0.5, 10, 20, 30, 50, and 100 Hz). Endurance index was calculated as the ratio of Pdi generated after 30s of phrenic nerve stimulation at 10 Hz divided by the initial force. Measurements of lung weights and lung histologic examinations were performed in the 6 remaining rats from each group. S animals were hyperthermic (39 to 40.degree. C rectal temperature). There was no evidence of pneumonia at histologic examination in Group S. No differences in wet weight of the lung and in the dry-to-wet weight ratio were noted in Group S as compared with Group C. However, S. pneumoniae was isolated from blood and lungs of S animals. Diaphragmatic weight was not different between S and C groups, whereas the weights of the extensor digitorium longus (EDL), tibialis anterior (TA), and soleus muscles were significantly reduced in Group S as compared to Group C. Diaphragmatic strength was reduced in Group S compared with Group C, as assessed by the reduction in Pdi for all frequencies of stimulation except 30 Hz. This altered diaphragmatic strength in S group was associated with an increase in the rate of relaxation of the twitch Pdi when compared to C group (S: 22.48 .+-. 3 ms; C: 15.60 .+-. ms; p < 0.001) and a reduced endurance performance as assessed by a lower diaphragmatic endurance index (S: 0.73 .+-. 0.05; C: 0.99 .+-. 0.04; p < 0.01). We conclude that acute sepsis produces (1) a decrease in diaphragmatic strength related to an impaired contractility, and (2) a reduction in diaphragmatic endurance capacity.